Enter Yossarian: How to Resolve the Procedural Catch-22 That the Private Securities Litigation Reform Act Creates

Section II of this Article sets forth our understanding of what the Reform Act requires a plaintiff to set forth in a complaint to state a valid claim that a corporation has made false or misleading public statements in violation of section 10(b) and Rule 10(b)(5). Section III describes our case study of GTF. Section IV analyzes the options a court would face in a case similar to the quasi-hypothetical we studied and suggests the option we believe a court should choose

Murid herpesvirus-4 lacking thymidine kinase reveals route-dependent requirements for host colonization

Gammaherpesviruses infect at least 90 % of the world's population. Infection control is difficult, in part because some fundamental features of host colonization remain unknown, for example whether normal latency establishment requires viral lytic functions. Since human gammaherpesviruses have narrow species tropisms, answering such questions requires animal models. Murid herpesvirus-4 (MuHV-4) provides one of the most tractable. MuHV-4 genomes delivered to the lung or peritoneum persist without lytic replication. However, they fail to disseminate systemically, suggesting that the outcome is inoculation route-dependent. After upper respiratory tract inoculation, MuHV-4 infects mice without involving the lungs or peritoneum. We examined whether host entry by this less invasive route requires the viral thymidine kinase (TK), a gene classically essential for lytic replication in terminally differentiated cells. MuHV-4 TK knockouts delivered to the lung or peritoneum were attenuated but still reached lymphoid tissue. In contrast, TK knockouts delivered to the upper respiratory tract largely failed to establish a detectable infection. Therefore TK, and by implication lytic replication, is required for MuHV-4 to establish a significant infection by a non-invasive route

In vivo importance of heparan sulfate-binding glycoproteins for murid herpesvirus-4 infection

Many herpesviruses bind to heparan sulfate (HS). Murid herpesvirus-4 (MuHV-4) does so via its envelope glycoproteins gp70 and gH/gL. MuHV-4 gp150 further regulates an HS-independent interaction to make that HS-dependent too. Cell binding by MuHV-4 virions is consequently strongly HS-dependent. Gp70 and gH/gL show some in vitro redundancy: an antibody-mediated blockade of HS binding by one is well tolerated, whereas a blockade of both severely impairs infection. In order to understand the importance of HS binding for MuHV-4 in vivo, we generated mutants lacking both gL and gp70. As expected, gL−gp70− MuHV-4 showed very poor cell binding. It infected mice at high dose but not at low dose, indicating defective host entry. But once entry occurred, host colonization, which for MuHV-4 is relatively independent of the infection dose, was remarkably normal. The gL−gp70− entry deficit was much greater than that of gL− or gp70− single knockouts. And gp150 disruption, which allows HS-independent cell binding, largely rescued the gL−gp70− cell binding and host entry deficits. Thus, it appeared that MuHV-4 HS binding is important in vivo, principally for efficient host entry

The Vehicle, Spring 1993

1993 Commemorative Edition: Celebrating 35 Years Table of Contents The Vehicle Editors\u27 Lineagepage 5 Milestonespage 6 THE SIXTIES Coverspage 7 Editors\u27 Notespage 8 Sureness is Never - excerptDon Shepardsonpage 9 SophisticationBenjamin Polkpage 10 A SonnetMignon Stricklandpage 11 The Twenty-Third ChannelBen Polkpage 11 Opposite AttractionsC.E.M. (Christine McColl)page 12 John F. KennedyJoel E. Hendrickspage 13 The Girl on the White PonyLarry Gatespage 14 The TimesW.D.M. (William Moser)page 16 Home ThoughtsJane Careypage 17 1966Roger Zulaufpage 18 Nagging ThoughtJanet Andrewspage 18 THE SEVENTIES Coverspage 19 Editors\u27 Notespage 20 RevolutionsSteve Siegelpage 21 UntitledKristine Kirkhampage 23 The Arithmetic ProblemJanice Forbuspage 23 Willie Seeverson Threw a Worm at MeMary Pipekpage 24 a love poem (by approximation)Ted Baldwinpage 25 Night and Summer in Two WorldsBarry Smithpage 26 Story of a Teenage PickleTerry Louis Schultzpage 27 Danny Lonely, Danny WildDevin Brownpage 28 Always TomorrowMary McDanielpage 29 THE EIGHTIES Coverspage 31 Having ChildrenDevon Flesorpage 33 What is Unnatural Is Sometimes MagicAngelique Jenningspage 34 If My Father Were A Writer, He Would Still BuildAngelique Jenningspage 35 Photo AlbumPatrick Peterspage 36 Poet Born in Pearl HarborAngelique Jenningspage 37 The History of High School BasketballPatrick Peterspage 38 Banana BreadGail Bowerpage 39 Cover LetterBob Zordanipage 40 Home MoviesBob Zordanipage 41 MigrationPatrick Peterspage 42 THE NINETIES Ba, Ba, Black SheepVictoria Bennettpage 45 Daily LessonsJennifer Moropage 49 Folding My OwnLaurie Ann Malispage 51 About the Authorspage 53 Editors\u27 Notespage 56https://thekeep.eiu.edu/vehicle/1062/thumbnail.jp

Persistence of accuracy of genomic estimated breeding values over generations in layer chickens

<p>Abstract</p> <p>Background</p> <p>The predictive ability of genomic estimated breeding values (GEBV) originates both from associations between high-density markers and QTL (Quantitative Trait Loci) and from pedigree information. Thus, GEBV are expected to provide more persistent accuracy over successive generations than breeding values estimated using pedigree-based methods. The objective of this study was to evaluate the accuracy of GEBV in a closed population of layer chickens and to quantify their persistence over five successive generations using marker or pedigree information.</p> <p>Methods</p> <p>The training data consisted of 16 traits and 777 genotyped animals from two generations of a brown-egg layer breeding line, 295 of which had individual phenotype records, while others had phenotypes on 2,738 non-genotyped relatives, or similar data accumulated over up to five generations. Validation data included phenotyped and genotyped birds from five subsequent generations (on average 306 birds/generation). Birds were genotyped for 23,356 segregating SNP. Animal models using genomic or pedigree relationship matrices and Bayesian model averaging methods were used for training analyses. Accuracy was evaluated as the correlation between EBV and phenotype in validation divided by the square root of trait heritability.</p> <p>Results</p> <p>Pedigree relationships in outbred populations are reduced by 50% at each meiosis, therefore accuracy is expected to decrease by the square root of 0.5 every generation, as observed for pedigree-based EBV (Estimated Breeding Values). In contrast the GEBV accuracy was more persistent, although the drop in accuracy was substantial in the first generation. Traits that were considered to be influenced by fewer QTL and to have a higher heritability maintained a higher GEBV accuracy over generations. In conclusion, GEBV capture information beyond pedigree relationships, but retraining every generation is recommended for genomic selection in closed breeding populations.</p

The Vehicle, Spring 1993

1993 Commemorative Edition: Celebrating 35 Years Table of Contents The Vehicle Editors\u27 Lineagepage 5 Milestonespage 6 THE SIXTIES Coverspage 7 Editors\u27 Notespage 8 Sureness is Never - excerptDon Shepardsonpage 9 SophisticationBenjamin Polkpage 10 A SonnetMignon Stricklandpage 11 The Twenty-Third ChannelBen Polkpage 11 Opposite AttractionsC.E.M. (Christine McColl)page 12 John F. KennedyJoel E. Hendrickspage 13 The Girl on the White PonyLarry Gatespage 14 The TimesW.D.M. (William Moser)page 16 Home ThoughtsJane Careypage 17 1966Roger Zulaufpage 18 Nagging ThoughtJanet Andrewspage 18 THE SEVENTIES Coverspage 19 Editors\u27 Notespage 20 RevolutionsSteve Siegelpage 21 UntitledKristine Kirkhampage 23 The Arithmetic ProblemJanice Forbuspage 23 Willie Seeverson Threw a Worm at MeMary Pipekpage 24 a love poem (by approximation)Ted Baldwinpage 25 Night and Summer in Two WorldsBarry Smithpage 26 Story of a Teenage PickleTerry Louis Schultzpage 27 Danny Lonely, Danny WildDevin Brownpage 28 Always TomorrowMary McDanielpage 29 THE EIGHTIES Coverspage 31 Having ChildrenDevon Flesorpage 33 What is Unnatural Is Sometimes MagicAngelique Jenningspage 34 If My Father Were A Writer, He Would Still BuildAngelique Jenningspage 35 Photo AlbumPatrick Peterspage 36 Poet Born in Pearl HarborAngelique Jenningspage 37 The History of High School BasketballPatrick Peterspage 38 Banana BreadGail Bowerpage 39 Cover LetterBob Zordanipage 40 Home MoviesBob Zordanipage 41 MigrationPatrick Peterspage 42 THE NINETIES Ba, Ba, Black SheepVictoria Bennettpage 45 Daily LessonsJennifer Moropage 49 Folding My OwnLaurie Ann Malispage 51 About the Authorspage 53 Editors\u27 Notespage 56https://thekeep.eiu.edu/vehicle/1062/thumbnail.jp

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Sex differences in in-hospital mortality following a first acute myocardial infarction: Symptomatology, delayed presentation, and hospital setting

Background: Women generally wait longer than men prior to seeking treatment for acute myocardial infarction (AMI). They are more likely to present with atypical symptoms, and are less likely to be admitted to coronary or intensive care units (CCU or ICU) compared to similarly-aged males. Women are more likely to die during hospital admission. Sex differences in the associations of delayed arrival, admitting ward, and mortality have not been thoroughly investigated. Methods: Focusing on presenting symptoms and time of presentation since symptom onset, we evaluated sex differences in in-hospital mortality following a first AMI in 4859 men and women presenting to three emergency departments (ED) from December 2008 to February 2014. Sex-specific risk of mortality associated with admission to either CCU/ICU or medical wards was calculated after adjusting for age, socioeconomic status, triage-assigned urgency of presentation, blood pressure, heart rate, presenting symptoms, timing of presentation since symptom onset, and treatment in the ED. Sex-specific age-adjusted attributable risks were calculated.Results: Compared to males, females waited longer before seeking treatment, presented more often with atypical symptoms, and were less likely to be admitted to CCU or ICU. Age-adjusted mortality in CCU/ICU or medical wards was higher among females (3.1 and 4.9 % respectively in CCU/ICU and medical wards in females compared to 2.6 and 3.2 % in males). However, after adjusting for variation in presenting symptoms, delayed arrival and other risk factors, risk of death was similar between males and females if they were admitted to CCU or ICU. This was in contrast to those admitted to medical wards. Females admitted to medical wards were 89 % more likely to die than their male counterparts. Arriving in the ED within 60 min of onset of symptoms was not associated with in-hospital mortality. Among males, 2.2 % of in-hospital mortality was attributed to being admitted to medical wards rather than CCU or ICU, while for females this age-adjusted attributable risk was 4.1 %. Conclusions: Our study stresses the need to reappraise decision making in patient selection for admission to specialised care units, whilst raising awareness of possible sex-related bias in management of patients diagnosed with an AMI

Murid Herpesvirus-4 Exploits Dendritic Cells to Infect B Cells

Dendritic cells (DCs) play a central role in initiating immune responses. Some persistent viruses infect DCs and can disrupt their functions in vitro. However, these viruses remain strongly immunogenic in vivo. Thus what role DC infection plays in the pathogenesis of persistent infections is unclear. Here we show that a persistent, B cell-tropic gamma-herpesvirus, Murid Herpesvirus-4 (MuHV-4), infects DCs early after host entry, before it establishes a substantial infection of B cells. DC-specific virus marking by cre-lox recombination revealed that a significant fraction of the virus latent in B cells had passed through a DC, and a virus attenuated for replication in DCs was impaired in B cell colonization. In vitro MuHV-4 dramatically altered the DC cytoskeleton, suggesting that it manipulates DC migration and shape in order to spread. MuHV-4 therefore uses DCs to colonize B cells